Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen

Wu, Jianxiong; Zhang, Hongjun; Deng, Rulin; Hu, Mingwu; Fu, Xiaoling

doi:10.3892/mmr.2021.12453

Cited by 5 publications

(3 citation statements)

References 31 publications

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“…Additionally, we also detected the level of FGF18, which is a typical downstream effector of miR-21-5p. As reported by previous studies, the variants in FGF18 gene would induce bone disorders and the impaired function of the gene by different miRs promoted the development of OA (Jiang et al, 2021;Joob & Wiwanitkit, 2020;Wu, Zhang, et al, 2021). Collectively, changes in miR-21-5p/FGF18 axis would provide a preliminary explanation on the anti-OA function of Rb1: the compound benefits joint tissues by suppressing inflammation and increasing chondrocyte viability, which is exerted by inducing the level of FGF18 via the inhibition of miR-21-5p.…”

Section: Discussionmentioning

confidence: 70%

Ginsenoside Rb1 from Panax ginseng attenuates monoiodoacetate‐induced osteoarthritis by inhibiting miR ‐21‐5p/ FGF18 ‐mediated inflammation

Luan

Che²,

et al. 2022

Journal of Food Biochemistry

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Osteoarthritis (OA) is a major degenerative disorder that affects the knee, and more than 33.6% of people aged over 65 years are affected by the disorder (O'Connor, 2006;Srikanth et al., 2005). The typical symptoms associated with OA include pain, swelling, stiffness, and loss of weight-bearing joint flexibility, all of which cast great burdens on patients' lives and the public health system. Currently, the most commonly used therapies for OA are those based on rehabilitation exercises and medication. However, these conventional therapies aim more at attenuating symptoms rather than providing curative treatment. Additionally, for patients with end-stage OA, joint replacement surgery is the only effective strategy, although the surgery itself comes with disadvantages such as high associated costs, perioperative complications, and infections (Gunaratne et al., 2017). Thus, the development of mild and effective methods of handling OA is highly solicited.

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Section: Discussionmentioning

confidence: 70%

Ginsenoside Rb1 from Panax ginseng attenuates monoiodoacetate‐induced osteoarthritis by inhibiting miR ‐21‐5p/ FGF18 ‐mediated inflammation

Luan

Che²,

et al. 2022

Journal of Food Biochemistry

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“…Rat chondrocytes were isolated from femoral heads of healthy Sprague–Dawley (SD) rats following previously published methods (Wu et al, 2021). The isolated chondrocytes were then subjected to 4 μM of MIA for 24 h to induce OA symptoms and treated with 10 μM nardosinone for 24 h (Figure S1).…”

Section: Methodsmentioning

confidence: 99%

“…published methods (Wu et al, 2021). The isolated chondrocytes were then subjected to 4 μM of MIA for 24 h to induce OA symptoms and treated with 10 μM nardosinone for 24 h (Figure S1).…”

Section: Isolation Of Chondrocytes and Microarray Detectionmentioning

confidence: 99%

Nardosinone suppresses monoiodoacetate‐induced osteoarthritis in rats: The key role of the miR‐218‐5p/NUMB axis

Luo²,

Zhang

2022

Chem Biol Drug Des

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Nardosinone is a bioactive compound with a sesquiterpenoid structure isolated from Nardostachys jatamansi. The compound has shown treatment effects against skeletal disorders. In the current study, the effects of nardosinone on osteoarthritis (OA) were first assessed and the mechanism underlying the effects was explored by detecting changes in the miR‐218‐5p/NUMB axis. The miR, as a potential target mediating the effects of nardosinone on OA, was first determined with microarray and RT‐qPCR detections. Then, OA symptoms were induced in rats using monoiodoacetate (MIA) and treated with nardosinone. The anti‐OA effects of nardosinone were assessed via the detection of the histological structure and inflammation. The role of miR‐218‐5p was delineated by modulating its levels in OA‐affected rats. Based on the results of microarray and RT‐qPCR detections, miR‐218‐5p was selected as the therapeutic target for nardosinone. The induction of OA resulted in tissue destruction and the production of cytokines in rat joint tissues, which was associated with the up‐regulation of miR‐218‐5p and the downregulation of NUMB. For OA‐affected rats treated with nardosinone, the joint structure was improved and the inflammatory response was suppressed, along with the restored expression levels of miR‐218‐5p and NUMB. The re‐induced level of miR‐218‐5p compromised the anti‐OA effects of nardosinone, indicating that the inhibition of the miR played an indispensable role in the anti‐OA function of nardosinone. Collectively, the findings of our study demonstrated that nardosinone exerts treatment effects against OA by modulating the miR‐218‐5p/NUMB axis. Future studies will provide more detailed information on the interaction between nardosinone and miR in the attenuation of OA.

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Autophagy-related genes and pathways was associated with osteoarthritis pathogenesis

Guan

Guo

et al. 2023

Preprint

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Background: Patients with osteoarthritis have musculoskeletal-related chronic disability, leading to the high pain intensity. Explaining the molecular mechanisms of osteoarthritis is critial for the diagnosis and cure. Therefore, This research aimed to find key candidate genes involved in osteoarthritis pathogenesis. Methods: We identified differentially expressed genes by integrating multiple microarry datasets in cartilage (GSE43923, GSE113825, GSE129147 and GSE169077). Functional enrichment analysis and protein-protein interaction analysis were performed. Results: We identified sixty-six significantly expression genes (56 up-regulated and 10 down-regulated). Through functional enrichment analysis and protein-protein interaction analysis, we found that the biological process of these genes was enriched in focal adhesion, ECM-receptor interaction and PI3K-Akt signaling, which were closely related with autophagy. Moreover, ceRNA network showed that thirty-four DEGs, including ECM-receptor interaction-related genes (COL4A1, COL4A2 and COL1A2, LAMB1 an THBS2), exist competing endogenous regulating network mediated by 7 lncRNAs and 8 miRNAs. Furthermore, differentially expressed autophagy-related genes (CCL2, CDKN1A, CXCR4, DAPK1, DLC1, FAS, HSPA8, MYC and SERPINA1) were remarkably identified to interact with multiple of the common DEGs in ECM-receptor interaction and PI3K-Akt signaling pathway, suggesting that autophagy plays important role in osteoarthritis pathogenesis by regulating ECM-receptor interaction and PI3K-Akt signaling pathway. Conclusions: This multiple transcriptome analysis identifies ECM-receptor interaction and PI3K-Akt signaling pathway related to osteoarthritis pathogenesis by regulating autophagy and participating in ceRNA network.

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Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen

Cited by 5 publications

References 31 publications

Ginsenoside Rb1 from Panax ginseng attenuates monoiodoacetate‐induced osteoarthritis by inhibiting miR ‐21‐5p/ FGF18 ‐mediated inflammation

Ginsenoside Rb1 from Panax ginseng attenuates monoiodoacetate‐induced osteoarthritis by inhibiting miR ‐21‐5p/ FGF18 ‐mediated inflammation

Nardosinone suppresses monoiodoacetate‐induced osteoarthritis in rats: The key role of the miR‐218‐5p/NUMB axis

Autophagy-related genes and pathways was associated with osteoarthritis pathogenesis

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